title: Severity of allergic airway disease due to house dust mite allergen is not increased after clinical recovery of lung infection with Chlamydia pneumoniae in mice.
abstract: Chlamydia pneumoniae is associated with chronic inflammatory lung diseases like bronchial asthma and chronic obstructive pulmonary disease. The existence of a causal link between allergic airway disease and C. pneumoniae is controversial. A mouse model was used to address the question of whether preceding C. pneumoniae lung infection and recovery modifies the outcome of experimental allergic asthma after subsequent sensitization with house dust mite (HDM) allergen. After intranasal infection, BALB/c mice suffered from pneumonia characterized by an increased clinical score, reduction of body weight, histopathology, and a bacterial load in the lungs. After 4 weeks, when infection had almost resolved clinically, HDM allergen sensitization was performed for another 4 weeks. Subsequently, mice were subjected to a methacholine hyperresponsiveness test and sacrificed for further analyses. As expected, after 8 weeks, C. pneumoniae-specific antibodies were detectable only in infected mice and the titer was significantly higher in the C. pneumoniae/HDM allergen-treated group than in the C. pneumoniae/NaCl group. Intriguingly, airway hyperresponsiveness and eosinophilia in bronchoalveolar lavage fluid were significantly lower in the C. pneumoniae/HDM allergen-treated group than in the mock/HDM allergen-treated group. We did observe a relationship between experimental asthma and chlamydial infection. Our results demonstrate an influence of sensitization to HDM allergen on the development of a humoral antibacterial response. However, our model demonstrates no increase in the severity of experimental asthma to HDM allergen as a physiological allergen after clinically resolved severe chlamydial lung infection. Our results rather suggest that allergic airway disease and concomitant cellular changes in mice are decreased following C. pneumoniae lung infection in this setting.
authors.affiliation: Institute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Hannover, Germany.
authors.forename: Pavel
authors.initials: P
authors.lastname: Dutow
authors.forename: Sandra
authors.initials: S
authors.lastname: Lingner
authors.forename: Robert
authors.initials: R
authors.lastname: Laudeley
authors.forename: Silke
authors.initials: S
authors.lastname: Glage
authors.forename: Heinz-Gerd
authors.initials: HG
authors.lastname: Hoymann
authors.forename: Anna-Maria
authors.initials: AM
authors.lastname: Dittrich
authors.forename: Beate
authors.initials: B
authors.lastname: Fehlhaber
authors.forename: Meike
authors.initials: M
authors.lastname: Müller
authors.forename: Armin
authors.initials: A
authors.lastname: Braun
authors.forename: Andreas
authors.initials: A
authors.lastname: Klos
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D001249:Asthma / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology / Q000382:microbiology; D023521:Chlamydophila Infections / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D004802:Eosinophilia / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D005260:Female; D008168:Lung / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D011014:Pneumonia / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D039981:Pyroglyphidae / Q000276:immunology*; D012141:Respiratory Tract Infections / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*
chemical_list: D000485:Allergens